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Acute cerebral ischemia triggers local and systemic immune response. The aims of this project was to assess the blood serum concentration of the markers of inflammation and markers of the blood brain barrier damage on the first day of ischemic stroke, and the mutual correlations between these marker levels. Patients with first-in-life stroke were analysed according to: plasma concentration of the following markers on the first day of stroke: interleukin 2 (IL-2) and interleuki 6 (IL-6), S100B, tumor necrosis factor-α (TNF-α), progranulin (GRN), neuron specific enolase (NSE), urokinase-type plasminogen activator (uPA), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), C-reactive protein (CRP), leucocyte and thrombocyte counts; their neurological status on the first day of stroke (NIHSS) and their functional status at 30 days following stroke (mRS). The study included 138 patients with mean age: 73.11 ± 11.48. Patients with a higher score on the NIHSS showed significantly higher concentrations of TNF-α, white blood cells (WBC), CRP, NSE, IL-6 and S100B. Patients with a higher score on the modified Rankin Score (mRS) showed significantly higher concentrations of WBC, CRP, GRN, IL-6, S100B. Factors with an independent influence on the neurological status on the first day of stroke were: sex, WBC, total blood platelet (PLT) count, CRP, S100B and IL-6 levels. Atrial fibrillation, leukocyte count, CRP, NSA, uPA, IL-6 and S100B showed an independent impact on the functional status on the 30 th day of stroke. Patients with symptomatic atherosclerosis, as compared to others, were older (P = 0.003) and had higher levels of CRP, IL-6, and S100B. In each case, the differences were statistically significant. We conclude that the concentration of Il-6 and S100B on the first day of stroke are important for both the neurological status and the functional status in the acute period of the disease. Increased CRP and leukocyte count are associated with a worse prognosis regarding the course of acute stroke. The expression of pro-inflammatory agents and markers of blood-brain barrier damage in the acute phase of stroke seem to be more prominent in patients with symptomatic atherosclerosis than in patients with no clinical features of atherosclerosis. The expression of inflammatory parameters may indicate the importance of the inflammatory process starting during the early days of ischemic stroke, for the post-stroke neurological deficit.

The results of available studies on assessment of neurodegenerative lesions in multiple sclerosis (MS) patients using different approaches have not been conclusive. Currently, clinical assessment is the most commonly used (involving primarily mobility assessment), along with magnetic resonance imaging and electrophysiological testing. In this review we describe available clinical, neuroimaging, electrophysiological and laboratory tests used to assess the neurodegeneration in MS. Laboratory markers to determine the risk of disease, its conversion and prognosis in MS patients are being constantly sought. Cerebrospinal fluid (CSF) sample collection is invasive and constitutes a burden to a patient, so serum biomarkers are being investigated. Optimistic preliminary results of studies assessing neurofilament light chains (NFL) in serum of MS patients, encourage further research. The possibility to use such marker (or a group of markers) would significantly facilitate clinical decisions at the stage of diagnosis and treatment. Currently used treatments have limited efficacy and are associated with numerous adverse effects. Additional information from available clinical, imaging, electrophysiological or laboratory biomarker or a group of biomarkers, which predict the course and prognosis, will facilitate choosing optimal treatment and its escalation at the relevant stage. Conclusion: Using the diagnostic panel consisting of imaging, neurophysiology and serology testing along with clinical and neuropsychological assessment may improve the reliability of diagnostic instruments evaluating cerebral atrophy in MS patients. [ABSTRACT FROM AUTHOR]

Background and Objective: This study was conducted to evaluate the diagnostic performance of various biomarkers for steatosis, fibrosis, and inflammation in comparison to a liver biopsy (LB) in patients with nonalcoholic fatty liver disease (NAFLD). Materials and Methods: This was a cross-sectional study that included 135 patients with biopsy-proven NAFLD. Fatty liver index (FLI), hepatic steatosis index (HSI), cell death markers (CK-18 M30 and CK-18 M65), FIB-4 index, NAFLD fibrosis score (NFS), BARD, and AST to platelet ratio index (APRI) were calculated and analysed. Results: FLI, HSI scores, and the cell death biomarkers showed poor diagnostic accuracy for steatosis detection and quantification, with an area under the curve (AUC) of 0.7) for advanced fibrosis, whereas FIB-4, BARD, and NFS scores demonstrated poor performance (AUC < 0.70). However, a combination of FIB-4 and NFS with the cell death biomarkers had moderate accuracy for advanced (≥F3) fibrosis detection, with an AUC of >0.70. Conclusions: In this first study on Croatian patients with NAFLD, serum biomarkers demonstrated poor diagnostic performance for the noninvasive diagnosis of liver steatosis and NASH. APRI and the cell death biomarkers had only moderate accuracy for diagnosing advanced fibrosis, as did the combination of FIB-4 and NFS with the cell death biomarkers. Further studies regarding serum biomarkers for all NAFLD stages are needed.